Overexpression of the Renin-Angiotensin System in Human Visceral Adipose Tissue in Normal and Overweight Subjects

Giacchetti, Gilberta; Faloia, Emanuela; Mariniello, Barbara; Sardu, C.; Gatti, Cristina; Camilloni, Maria Angela; Guerrieri, Mario; Mantero, Franco

doi:10.1016/s0895-7061(02)02257-4

Cited by 170 publications

(128 citation statements)

References 27 publications

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“…Obesity leads to hypertension and increases the cardiovascular risk (Mikhail et al, 1999). RAS has been implicated in obesity by several authors (Giacchetti et al, 2002), which is supported by recent investigations that show high plasma concentrations of angiotensinogen (ANG) (Umemura et al, 1997) and a rise in the expression of the ANG gene in obese humans (Van Harmelen et al, 2000). The plasma ANG decrease was highly correlated with the WC decline and with one reduction in the systolic ambulatory blood pressure (Engeli et al, 2005).…”

Section: Discussionmentioning

confidence: 85%

Association between angiotensin-1 converting enzyme gene polymorphism and the metabolic syndrome in a Mexican population

et al. 2007

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Metabolic Syndrome (MS) is recognized as a cluster of cardiovascular risk factors. All components of MS have a genetic base. Genes of the renin angiotensin system are potential candidate genes for MS. We investigated whether angiotensin converting enzyme (ACE) gene polymorphism increases susceptibility to MS as an entity in a Mexican population. In a cross-sectional study, 514 individuals were studied including 245 patients with MS and 269 subjects without MS criteria. ACE gene polymorphism was detected using PCR. MS was defined according to The National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) criteria, except that the raised fasting plasma glucose ≥ 100 mg/dl criterion for identification of intolerance fasting glucose was modified in accordance with the suggestion of the American Diabetes Association. Patients with MS were significantly different from subjects without MS in relation to mean body mass index (BMI), waist circumference (WC), systolic blood pressure, diastolic blood pressure, glucose, total cholesterol (C), triglycerides, HDL-C, and LDL-C (P ＜ 0.0001). The differences in the mean BMI, WC, glucose, total cholesterol, triglycerides, LDL-C, and HDL-C were maintained in patients with the MS and DD genotypes (P ＜ 0.01). The DD genotype was strongly associated with MS (adjusted OR = 5.48, 95% CI 3.20-9.38, P ＜ 0.0001). We concluded that the DD genotype increases susceptibility to MS in a Mexican population. These results indicate that pharmacological and non-pharmacological treatment and a reduction in body fat will have important therapeutic implications in this disease.

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Section: Discussionmentioning

confidence: 85%

Association between angiotensin-1 converting enzyme gene polymorphism and the metabolic syndrome in a Mexican population

et al. 2007

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“…We can, however, not exclude that other proinflammatory mediators (such as angiotensin) 23 are released from visceral adipose tissue and result in the induction of PAI-1 release outside the fat compartment. Considering the vast and rapid induction of PAI-1 release from adipose tissue explants after exposure to proinflammatory stimuli (including angiotensin, Lindeman et al, unpublished data) and lack of PAI-1 release from adipose tissue in vivo, we consider such a mechanism unlikely.…”

Section: Discussionmentioning

confidence: 90%

Human visceral adipose tissue and the plasminogen activator inhibitor type 1

Lindeman

Pijl

Toet³

et al. 2007

Int J Obes

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Objective: The objective of this study was to systematically evaluate the molecular basis of the association between visceral fat mass and plasma plasminogen activator inhibitor-1 (PAI-1) levels in man. Design: A comprehensive approach comprising observational, in vitro, and human intervention studies. Measurements and results:We confirmed an exclusive relationship between visceral fat and plasma PAI-1 levels (r ¼ 0.79, Po0.001) and corroborated preferential PAI-1 release from adipose tissue explants. Yet, messenger RNA analysis and in vivo measurement of PAI-1 release from visceral fat (AV-differences over the omentum) not only excluded visceral adipose tissue as a relevant source of circulating PAI-1, but also excluded visceral fat as a significant source of proinflammatory mediators such as tumor necrosis factor-a, IL-1 or transforming growth factor-b that could induce PAI-1 expression in tissues other than visceral fat. Short-term interventions with acipimox and growth hormone (GH) as well as statistical evaluation excluded free fatty acids and GH as metabolic links. Further analysis of the metabolic data in a stepwise regression model indicated that plasma PAI-1 levels and visceral fat rather are co-correlates that both relate to impaired lipid handling. Conclusion: Our PAI-1 studies show that visceral fat mass and plasma PAI-1 levels are co-correlated rather than causatively related, with lipid load as common denominator.

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“…10 The main components of the tissue RAS systems, which can generate angiotensin II and other active peptides independently of circulating RAS components, are expressed in both visceral and subcutaneous adipose tissue. 32 Although the exact role of angiotensin II in adipose tissue is not yet clear, it has been shown to promote adipocyte growth and differentiation and can inhibit lipolysis by reducing skeletal and adipose-tissue blood flow leading to increased fat storage in normal-weight and obese subjects. 33 Furthermore, angiotensin II has been shown to increase lipid synthesis and storage in adipose cells in vitro 13 and therefore, may play an important role in growth and differentiation of this tissue.…”

Section: Discussionmentioning

confidence: 99%

Developmental changes in adiposity in toddlers and preschoolers in the GENESIS study and associations with the ACE I/D polymorphism

et al. 2007

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Objectives: To investigate the relationship between the angiotensin I-converting enzyme 1 (ACE) I/D polymorphism and adiposity-related phenotypes in a large cohort of toddlers and preschoolers. Methods: Body composition measurements and DNA samples were obtained from 2102 Greek children aged 1-6 years, as part of a large-scale epidemiological study (GENESIS). All children were genotyped for the ACE I/D polymorphism and gender-and age-stratified statistical analyses were performed. Results: In girls aged 4-6 years, the D-allele was associated with higher measurements of body mass index (BMI) (P ¼ 0.018), waist (P ¼ 0.001) and upper arm (P ¼ 0.013) circumferences, genotype accounting for 2.5, 4 and 3% of the phenotypic variance, respectively. In boys, the D-allele showed strong associations with lower BMI (P ¼ 0.001) at the age of 1-2 years that explained 17% of the phenotypic variance and with larger suprailiac skinfold (P ¼ 0.008) at 3-4 years old that explained 2% of the variance. No other significant associations between the ACE I/D polymorphism and adiposity-related phenotypes were found. In girls, the age at which significant associations were revealed coincided with the age at which BMI was observed to increase after its developmental nadir, but this feature of the association was not observed in boys. Conclusions: The ACE I/D polymorphism is associated with developmental and physiological changes in adiposity-related traits during early childhood in a gender-and age-specific manner.

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Overexpression of the Renin-Angiotensin System in Human Visceral Adipose Tissue in Normal and Overweight Subjects

Cited by 170 publications

References 27 publications

Association between angiotensin-1 converting enzyme gene polymorphism and the metabolic syndrome in a Mexican population

Association between angiotensin-1 converting enzyme gene polymorphism and the metabolic syndrome in a Mexican population

Human visceral adipose tissue and the plasminogen activator inhibitor type 1

Developmental changes in adiposity in toddlers and preschoolers in the GENESIS study and associations with the ACE I/D polymorphism

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